Persichino et al. BMC Infectious Diseases (2016) 16:375 DOI 10.1186/s12879-016-1752-3
CASE REPORT
Open Access
Effusive-constrictive pericarditis, hepatitis, and pancreatitis in a patient with possible coxsackievirus B infection: a case report Jon Persichino1*, Roger Garrison1, Rajagopal Krishnan2 and Made Sutjita3
Abstract Background: Coxsackie B is a viral pathogen that presents with various invasive diseases in adults. Historically, the majority of adult cases with pericarditis or myocarditis have been attributed to coxsackievirus B. The presentation of this viral infection causing effusive-constrictive pericarditis, hepatitis or pancreatitis is rare. This case report is the first to describe a patient with concomitant effusive-constrictive pericarditis, hepatitis and pancreatitis from possible coxsackievirus B infection. Case presentation: A 26-year old female was admitted to our hospital with the diagnosis of effusive-constrictive pericarditis complicated by tamponade and cardiac arrest. An emergent pericardiocentesis was performed successfully. Hepatitis and pancreatitis were also identified in our patient. After an extensive workup, coxsackievirus B infection was suspected by positive serum complement fixation antibody titers. Our patient made a full recovery and was discharged from the hospital. Conclusion: Clinical suspicion of effusive-constrictive pericarditis with tamponade from coxsackievirus B should be considered in patients presenting with chest pain, dyspnea, jugular venous distention, hypotension, ST segment elevation on electrocardiogram, and ventricular interdependence with septal shift during diastole on transthoracic echocardiogram. Initial diagnoses of effusive-constrictive pericarditis resembling cardiac tamponade, hepatitis and pancreatitis can be challenging, and this case highlights the need for healthcare professionals to be cognizant of the association between these unusual clinical presentations and coxsackievirus B infection. Keywords: Coxsackie B, Effusive-constrictive pericarditis, Hepatitis, Pancreatitis
Background Coxsackievirus, a RNA Enterovirus, has been traditionally associated with a number of clinical diseases in children and adults. The species is divided into two groups and 29 serotypes [1]. Coxsackie group A viruses can cause aseptic meningitis in adults, and commonly infect skin and mucous membranes in herpangina, conjunctivitis and hand, foot and mouth disease in children [1]. Group B viruses cause herpangina, pleurodynia, and infect the heart, pancreas, and liver which can give rise to myocarditis, pericarditis, pancreatitis and hepatitis in adults [2]. Viral pericarditis is inflammation of the pericardium or the lining surrounding the heart that is * Correspondence: [email protected] 1 Department of Internal Medicine, Riverside University Health System Medical Center, 26520 Cactus Avenue, Moreno Valley, CA 92555, USA Full list of author information is available at the end of the article
caused by viral infections [2]. Coxsackie B viruses are the most common cause of myocarditis and pericarditis in adults and have been identified in up to 50 % of viral cardiac cases [3–5]. A number of other viral, bacterial, and fungal infections as well as medications has also been shown to cause myocarditis and pericarditis [2, 6]. However, the presentation of this viral infection is rare among patients with isolated pancreatitis or hepatitis [7–11]. Up to 60 % of patients with acute pericarditis will develop a small pericardial effusion [6]. Notably, viral pericarditis can lead to pericardial constriction as a late complication [12, 13]. Constrictive pericarditis with effusion has been detected in ten percent of patients with clinical tamponade [2]. Coxsackie B viruses usually cause various single organ system diseases, but the combination of myocarditis, pancreatitis and hepatitis has been documented in two case reports [14, 15]. Herein,
© 2016 The Author(s). Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Persichino et al. BMC Infectious Diseases (2016) 16:375
Page 2 of 6
we report a case of possible coxsackievirus B infection causing effusive-constrictive pericarditis, hepatitis and pancreatitis.
Case presentation A 26-year old Latina female sought medical attention at our emergency department with progressive throat pain and chest pain for 1 week. She then developed fevers, dizziness, shortness of breath, and abdominal pain with nausea and vomiting 2 days prior to admission. She did not seek prior medical attention and used over-thecounter ibuprofen for the fevers. The patient denied any recent travel, unusual food consumption or animal exposures. Further history revealed that the patient’s 10-year old sister was recovering from an upper respiratory infection with fevers, throat pain, cough and shortness of breath for 1 week. Past medical history was significant for congenital adrenal hyperplasia. Our patient denied current usage of tobacco, alcohol, or intravenous drugs. She had no known drug allergies and had been taking physiologic doses of hydrocortisone 30 milligrams (mg) per day and fludrocortisone 0.5 mg per day for her congenital adrenal hyperplasia. The patient disclosed to the medical team that she had run out of her hydrocortisone and fludrocortisone approximately 4 to 6 weeks prior to admission. Initial vital signs in the emergency department demonstrated a temperature of 102.0 °F (38.9 °C), heart rate of 102 per minute, respiratory rate of 28 per minute, oxygen saturation of 95 % while breathing 6 liters of oxygen per minute via face mask, and blood pressure of 50/21 millimeters of mercury. On examination, she was ill appearing and diaphoretic. There was jugular venous distention by visualization of the neck veins and distant heart sounds upon auscultation. Aggressive intravenous fluid hydration, vasopressor medications, and intravenous hydrocortisone were initiated for suspected septic shock and adrenal crisis. Supplemental oxygen was
provided by face mask. Empiric antibiotic treatments with vancomycin, levofloxacin, fluconazole, and metronidazole were initiated based upon consultation with the infectious diseases specialist. Blood and urine cultures were collected in the emergency department before antibiotic administration. Pertinent laboratory findings in our patient on admission and during hospitalization are shown on Table 1. A 12-lead electrocardiogram (ECG) showed 1–2 mm ST segment elevations in precordial V2-V6 leads as shown in Fig. 1. Pericarditis with tamponade was suspected by the emergency room personnel. An emergent bedside transthoracic echocardiogram (TTE) was performed by a technician which revealed a small pericardial effusion. A portable chest radiograph was remarkable for vascular congestion only. Two hours after her arrival to the emergency department, the patient developed cardiac arrest. Adult cardiac life support was initiated in which intubation and cardiopulmonary resuscitation were performed. Intravenous epinephrine was given for pulseless electrical activity. Pulse was restored after three minutes of treatment. An emergent bedside pericardiocentesis with drain placement was carried out by the on-call cardiologist. Threehundred milliliters of serosanginous pericardial fluid were extracted. A repeat bedside TTE revealed minimal residual effusion of the pericardium with normal ventricular function. The patient was admitted to the intensive care unit with the diagnosis of effusive-constrictive pericarditis complicated by tamponade, cardiac arrest and adrenal crisis. Additional samples of blood and urine were collected for screening of bacterial (Streptococcus, Staphylococcus, Meningococcus, Haemophilus, Legionella), fungal (Histoplasma, Aspergillus, Candida, Cryptococcus, Coccidiomycosis), viral (herpesviruses, human immunodeficiency virus, Epstein-Barr virus, hepatitis A, B, and C, Cytomegalovirus), and mycobacterial (Mycobacterium tuberculosis, Mycobacterium avium complex) infections with negative results. Serological paired complement fixation
Table 1 Laboratory values in our patient on admission, during hospitalization, and post-hospital follow-up Normal value
Day 1
Day 4
Day 8
Day 12
Day 16
Follow-up After 4 weeks
TB
0.2–1.0 mg/dl
2.3
1.4
0.6
0.4
0.4
0.6
ALT
12–78 U/L
109
868
420
138
86
34
AST
15–37 U/L
213
1,060
189
21
22
29
CK
26–192 U/L
225
353
521
NR
NR
NR
CKMB
0.5–3.6 ng/ml
3.4
8.4
14.0
NR
NR
NR
Troponin
0.000–0.045 ng/ml
0.44
0.89
0.45
NR
NR
NR
Amylase
25–115 U/ml
102
212
NR
NR
NR
NR
Lipase
73–393 U/L
773
1,739
7,880
4,850
NR
262
TB total bilirubin, mg milligrams, dl deciliter, ALT alanine aminotransferase, U units, L liter, AST aspartate transaminase, CK creatinine kinase, CKMB creatinine kinase MB, ng nanograms, ml milliliter, NR no result
Persichino et al. BMC Infectious Diseases (2016) 16:375
Page 3 of 6
Fig. 1 Electrocardiogram from patient with ST-segment elevations (arrows) in V2-V4 precordial leads
antibody titers for coxsackie A and B were sent on days 1 and 7 of hospitalization. A panel of serological tests for rheumatologic, autoimmune and malignant diseases were performed as well. All pericardial fluid stains and cultures were negative for bacterial, fungal and mycobacterial diseases. Rheumatologic, autoimmune and malignancy workups were negative. Our infectious disease specialist suspected coxsackievirus infection given patient’s presentation and history of recent sick contact with her younger sister. Coxsackie titer antibodies were negative for group A serotypes A2, A4, A7, A9, A10 and A16. Coxsackie B titer antibodies on day 1 were: B1 (
CASE REPORT
Open Access
Effusive-constrictive pericarditis, hepatitis, and pancreatitis in a patient with possible coxsackievirus B infection: a case report Jon Persichino1*, Roger Garrison1, Rajagopal Krishnan2 and Made Sutjita3
Abstract Background: Coxsackie B is a viral pathogen that presents with various invasive diseases in adults. Historically, the majority of adult cases with pericarditis or myocarditis have been attributed to coxsackievirus B. The presentation of this viral infection causing effusive-constrictive pericarditis, hepatitis or pancreatitis is rare. This case report is the first to describe a patient with concomitant effusive-constrictive pericarditis, hepatitis and pancreatitis from possible coxsackievirus B infection. Case presentation: A 26-year old female was admitted to our hospital with the diagnosis of effusive-constrictive pericarditis complicated by tamponade and cardiac arrest. An emergent pericardiocentesis was performed successfully. Hepatitis and pancreatitis were also identified in our patient. After an extensive workup, coxsackievirus B infection was suspected by positive serum complement fixation antibody titers. Our patient made a full recovery and was discharged from the hospital. Conclusion: Clinical suspicion of effusive-constrictive pericarditis with tamponade from coxsackievirus B should be considered in patients presenting with chest pain, dyspnea, jugular venous distention, hypotension, ST segment elevation on electrocardiogram, and ventricular interdependence with septal shift during diastole on transthoracic echocardiogram. Initial diagnoses of effusive-constrictive pericarditis resembling cardiac tamponade, hepatitis and pancreatitis can be challenging, and this case highlights the need for healthcare professionals to be cognizant of the association between these unusual clinical presentations and coxsackievirus B infection. Keywords: Coxsackie B, Effusive-constrictive pericarditis, Hepatitis, Pancreatitis
Background Coxsackievirus, a RNA Enterovirus, has been traditionally associated with a number of clinical diseases in children and adults. The species is divided into two groups and 29 serotypes [1]. Coxsackie group A viruses can cause aseptic meningitis in adults, and commonly infect skin and mucous membranes in herpangina, conjunctivitis and hand, foot and mouth disease in children [1]. Group B viruses cause herpangina, pleurodynia, and infect the heart, pancreas, and liver which can give rise to myocarditis, pericarditis, pancreatitis and hepatitis in adults [2]. Viral pericarditis is inflammation of the pericardium or the lining surrounding the heart that is * Correspondence: [email protected] 1 Department of Internal Medicine, Riverside University Health System Medical Center, 26520 Cactus Avenue, Moreno Valley, CA 92555, USA Full list of author information is available at the end of the article
caused by viral infections [2]. Coxsackie B viruses are the most common cause of myocarditis and pericarditis in adults and have been identified in up to 50 % of viral cardiac cases [3–5]. A number of other viral, bacterial, and fungal infections as well as medications has also been shown to cause myocarditis and pericarditis [2, 6]. However, the presentation of this viral infection is rare among patients with isolated pancreatitis or hepatitis [7–11]. Up to 60 % of patients with acute pericarditis will develop a small pericardial effusion [6]. Notably, viral pericarditis can lead to pericardial constriction as a late complication [12, 13]. Constrictive pericarditis with effusion has been detected in ten percent of patients with clinical tamponade [2]. Coxsackie B viruses usually cause various single organ system diseases, but the combination of myocarditis, pancreatitis and hepatitis has been documented in two case reports [14, 15]. Herein,
© 2016 The Author(s). Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Persichino et al. BMC Infectious Diseases (2016) 16:375
Page 2 of 6
we report a case of possible coxsackievirus B infection causing effusive-constrictive pericarditis, hepatitis and pancreatitis.
Case presentation A 26-year old Latina female sought medical attention at our emergency department with progressive throat pain and chest pain for 1 week. She then developed fevers, dizziness, shortness of breath, and abdominal pain with nausea and vomiting 2 days prior to admission. She did not seek prior medical attention and used over-thecounter ibuprofen for the fevers. The patient denied any recent travel, unusual food consumption or animal exposures. Further history revealed that the patient’s 10-year old sister was recovering from an upper respiratory infection with fevers, throat pain, cough and shortness of breath for 1 week. Past medical history was significant for congenital adrenal hyperplasia. Our patient denied current usage of tobacco, alcohol, or intravenous drugs. She had no known drug allergies and had been taking physiologic doses of hydrocortisone 30 milligrams (mg) per day and fludrocortisone 0.5 mg per day for her congenital adrenal hyperplasia. The patient disclosed to the medical team that she had run out of her hydrocortisone and fludrocortisone approximately 4 to 6 weeks prior to admission. Initial vital signs in the emergency department demonstrated a temperature of 102.0 °F (38.9 °C), heart rate of 102 per minute, respiratory rate of 28 per minute, oxygen saturation of 95 % while breathing 6 liters of oxygen per minute via face mask, and blood pressure of 50/21 millimeters of mercury. On examination, she was ill appearing and diaphoretic. There was jugular venous distention by visualization of the neck veins and distant heart sounds upon auscultation. Aggressive intravenous fluid hydration, vasopressor medications, and intravenous hydrocortisone were initiated for suspected septic shock and adrenal crisis. Supplemental oxygen was
provided by face mask. Empiric antibiotic treatments with vancomycin, levofloxacin, fluconazole, and metronidazole were initiated based upon consultation with the infectious diseases specialist. Blood and urine cultures were collected in the emergency department before antibiotic administration. Pertinent laboratory findings in our patient on admission and during hospitalization are shown on Table 1. A 12-lead electrocardiogram (ECG) showed 1–2 mm ST segment elevations in precordial V2-V6 leads as shown in Fig. 1. Pericarditis with tamponade was suspected by the emergency room personnel. An emergent bedside transthoracic echocardiogram (TTE) was performed by a technician which revealed a small pericardial effusion. A portable chest radiograph was remarkable for vascular congestion only. Two hours after her arrival to the emergency department, the patient developed cardiac arrest. Adult cardiac life support was initiated in which intubation and cardiopulmonary resuscitation were performed. Intravenous epinephrine was given for pulseless electrical activity. Pulse was restored after three minutes of treatment. An emergent bedside pericardiocentesis with drain placement was carried out by the on-call cardiologist. Threehundred milliliters of serosanginous pericardial fluid were extracted. A repeat bedside TTE revealed minimal residual effusion of the pericardium with normal ventricular function. The patient was admitted to the intensive care unit with the diagnosis of effusive-constrictive pericarditis complicated by tamponade, cardiac arrest and adrenal crisis. Additional samples of blood and urine were collected for screening of bacterial (Streptococcus, Staphylococcus, Meningococcus, Haemophilus, Legionella), fungal (Histoplasma, Aspergillus, Candida, Cryptococcus, Coccidiomycosis), viral (herpesviruses, human immunodeficiency virus, Epstein-Barr virus, hepatitis A, B, and C, Cytomegalovirus), and mycobacterial (Mycobacterium tuberculosis, Mycobacterium avium complex) infections with negative results. Serological paired complement fixation
Table 1 Laboratory values in our patient on admission, during hospitalization, and post-hospital follow-up Normal value
Day 1
Day 4
Day 8
Day 12
Day 16
Follow-up After 4 weeks
TB
0.2–1.0 mg/dl
2.3
1.4
0.6
0.4
0.4
0.6
ALT
12–78 U/L
109
868
420
138
86
34
AST
15–37 U/L
213
1,060
189
21
22
29
CK
26–192 U/L
225
353
521
NR
NR
NR
CKMB
0.5–3.6 ng/ml
3.4
8.4
14.0
NR
NR
NR
Troponin
0.000–0.045 ng/ml
0.44
0.89
0.45
NR
NR
NR
Amylase
25–115 U/ml
102
212
NR
NR
NR
NR
Lipase
73–393 U/L
773
1,739
7,880
4,850
NR
262
TB total bilirubin, mg milligrams, dl deciliter, ALT alanine aminotransferase, U units, L liter, AST aspartate transaminase, CK creatinine kinase, CKMB creatinine kinase MB, ng nanograms, ml milliliter, NR no result
Persichino et al. BMC Infectious Diseases (2016) 16:375
Page 3 of 6
Fig. 1 Electrocardiogram from patient with ST-segment elevations (arrows) in V2-V4 precordial leads
antibody titers for coxsackie A and B were sent on days 1 and 7 of hospitalization. A panel of serological tests for rheumatologic, autoimmune and malignant diseases were performed as well. All pericardial fluid stains and cultures were negative for bacterial, fungal and mycobacterial diseases. Rheumatologic, autoimmune and malignancy workups were negative. Our infectious disease specialist suspected coxsackievirus infection given patient’s presentation and history of recent sick contact with her younger sister. Coxsackie titer antibodies were negative for group A serotypes A2, A4, A7, A9, A10 and A16. Coxsackie B titer antibodies on day 1 were: B1 (
